We have the CEO, Jonathan, and Yannis for Innate Pharma, and we are going to do a fireside chat. Could you provide an overview of Innate Pharma today and outline your strategic vision for growth? Yeah, so this is Jonathan here. So a basic overview of Innate Pharma. We're a company that specializes in proprietary antibodies, and out of that work have come a number of treatment modalities. We're focused on NK cell engagers as one pillar of our strategy. What we're basically doing is targeting NKp46 and CD16 on NK cells and putting a tumor tag onto that to produce a trispecific antibody. That's one of the pillars that we focus on. We also have ADCs, and again, we use that proprietary antibody technology to develop absolute best-in-class antibodies for those ADCs. We have a payload and some proprietary linker technology. We have a lead asset, IPH4502, which is in phase I today. We have a number of what I would call naked monoclonal antibodies, which are at various phases of development. The most advanced is Monalizumab, which is in a large phase III study in non-small cell lung cancer. We have another antibody targeting KIR3DL2, which is being developed in cutaneous T-cell lymphoma and has finished basically a phase II study and was recently given a breakthrough designation in Sézary syndrome by FDA. It's advancing very nicely on an accelerated path to approval. That's a quick overview of what the company's doing. For those less familiar, can you briefly describe the ANKET platform and its key differentiators? Yeah, so I think we'll let Yannis take this question. He's the expert on the platform. Yannis? Hi, good morning. Yeah, so we are having this NK cell engager platform that we are calling ANKET. It is a plug and play technology where we are building multispecific antibodies. To cut a long story short, in this molecule, there is one part of the molecule which is binding a tumor-associated antigen. That is a part that we can swap to target multiple antigen and then generate like that a series of different products. There is an invariant part, which is actually activating the NK cells. What makes our platform unique is the binding to the activating receptor called NKp46. We are the only ones to target that receptor, and we think that it is really the best one to activate NK cells because it is one which is very stable. The NK cells do have several activating receptors for targeting. When you look at the NK cell in the blood, but in the tissues, a lot of these activating receptors are downregulated or cleaved, which is not the case for NKp46. By targeting NKp46, we really maximize the number of NK cells that we can engage both in the blood, but also in the tissue, and especially in the tumor microenvironment. Thank you. How should we interpret Sanofi's recent $15 million equity investment in Innate, particularly in light of their decision to return IPH6101 rights? Yeah, I'll take this one. I think the way to interpret what Sanofi have done here is, I think we're all aware that they've had a strategic reprioritization and they're, to some degree, stepping back from oncology. I think you can see that on a number of the assets that they've been working with. IPH6101 was part of that strategic reprioritization, and they handed the rights back to us. At the same time, they place a lot of value on the ANKET platform and our ADCs and what we're doing at Innate. They have a lot of belief in those platforms. Hence, they made the $15 million strategic equity investment into the company. I think that reflects their confidence in the platform and their confidence in the science at Innate Pharma. They want to be still part of that for the future. What I would also mention is they retained the rights to the BCMA target and ANKET as part of that strategic reprioritization. They actually flipped the asset from oncology. It was being developed in myeloma, and they have put it into inflammation and autoimmunity. Off the back of that, we've not actually seen the results in myeloma, but we have to assume that they must look pretty good. The safety must be good, and we must be seeing a really good level of activity for them to want to reposition the asset into inflammation and autoimmunity. We take the return of the rights as a positive alongside the fact that they placed the $15 million equity investment into the company. Regarding returning these rights, can you provide some context into that decision and how it impacts your development plans for this asset? Yeah, that's a good question. In terms of how it affects our development plans, we don't have all of the data back from the product yet. According to the contract with Sanofi, they're obligated to provide us all of the clinical data from IPH6101 by the 1st of July. What we need to do is to take a look at that data, and then we'll be able to make some decisions on how we take that product forward. Just to remind you of the data that they've already presented, they were developing the product. It's targeting CD123. They were developing it in treatment refractory AML. They presented some very interesting data at EHA last year in the one milligram per kilogram dosing cohort, where they showed basically five complete responses out of 15 patients, so a 33% response rate in treatment refractory patients. They were durable responses, including one with MRD negativity. We take a lot of pride from that because I think that's validation of the ANKET platform and that actually targeting NK cells really works. We're excited to get the data back from Sanofi. We'll be taking a look at it, and then we'll be seeing what we need to do and where we need to take the asset. That will take us a little bit of time. I would guess sometime during the second half of the year, we'll be able to come up with a plan and communicate more on exactly what we're going to do. Sanofi is continuing to advance IPH6401. Can you update us on the progress there? Yeah, I can. IPH6401 was the product I mentioned earlier. This is the product targeting. It's an ANKET, so it's targeting the same NKp46 CD16. It has basically a BCMA tumor tag on it. It was being developed in myeloma by Sanofi in a phase I study, dose-finding study. They took the decision as part of their strategic reprioritization to pivot this asset into inflammation and autoimmunity. We don't know yet which particular indication they're going to be targeting. We'll find that out in due course. As I said earlier, again, the results in myeloma must have been good. It must be safe, and there must be good levels of efficacy for them to want to redirect it into the inflammation and autoimmunity space. Again, we'll be seeing some more information on that from Sanofi later in the year. It will be exciting to see how that's moving forward. I think from our perspective, again, this is a validation of the ANKET platform and the fact that this platform works and the fact that Sanofi is taking it into inflammation and autoimmunity also is good from our perspective because we have our own ANKETs that we're potentially going to take into inflammation and autoimmunity. I think this is giving us some proof of concept that this is the right way to go. Your proprietary tetraspecific ANKET IPH6501 is a novel approach. What makes it unique and when might we see initial clinical data? I think Yannis is going to take this one. Yeah, so like I said at the beginning, this new version, the IPH6501, is based on the same backbone of the entire platform with the one part, which is a binding portion that is targeting a tumor-associated antigen. There is a portion of the molecule activating the CD16 and this unique NKp46 engagement. What is new in this second version is that we have added, incorporated a cytokine, which is a variant of interleukin 2, which is allowing to induce the proliferation and expansion of the patient's own NK cells. That way, when the molecule binds to the NK cells, it induces their activation. It triggers the killing of the target, but also the expansion of the NK. Because in some disease, you may have a limited number of NK cells. With this new technology, we are expanding that number of cells that have this ability to kill the tumor cells. It's currently in phase I. We are in the dose escalation part of the phase I, and we should start having initial data, preliminary data by the end of the year. Thank you. So IPH4502 recently entered phase I with a trial in progress poster presented at ASCO. Can you tell us more about the design and goals of this trial? Again, I think Yannis will take this one. Yeah, so IPH4502 is our Nectin-4 Exatecan ADC. So it's a very differentiated molecule targeting this validated target that is Nectin-4. It's currently in a dose-escalating phase I. We have actually presented the design of the phase I at ASCO in a trial in progress poster. It's a very classical dose escalation with dose optimization portion. It's a trial where we are including up to nine different tumor types like bladder, and with the possibility also to include patients who have been pre-exposed to PADCEV, which is the approved drug targeting Nectin-4, but with a different payload, but also other major tumor types like non-small cell lung cancer, prostate, triple negative breast cancer, or colorectal cancer. It's currently ongoing. It's progressing extremely well. We have said that we have started the phase I in January, and we have said that in less than one week, we have completed the first dose level. It is currently moving fast with the same pace. We are, I would say, like for IPH6501, we are expecting preliminary data by the end of the year. In an increasingly competitive Nectin-4 ADC space, what differentiates IPH4502 from other programs? I think that there are actually two levels of differentiation. The first one is coming from the payload. Because as I mentioned, the approved drug, the PADCEV, the Enfortumab vedotin, is based on the MMAE payload. When you look at the competitive landscape, a lot of the next generation Nectin-4 targeting agents are based on the same technology, on the same payload, like the Bicycle molecules, the Mabwell, the Corbus. They are all using this MMAE as a payload. It comes with certain liability. As you know, one of the key liabilities for MMAE is peripheral neuropathy, which is a very important toxicity, which very often leads to a dose reduction or treatment interruption. These peripheral neuropathies are also irreversible. It is something that really is a problem for the patient. There is another problem that is related to the exposure to MMA and the fact that the first drug approved, which is now in first line in combination with Padcev in bladder, is that there is a major resistance mechanism that is triggered by the exposure to MMA, which is the upregulation of certain efflux pumps, the ABC transporter like MDR1, that are mediating the resistance to the MMA. It is something that has been described in the literature and that we have also observed in our own experiments. I mean, exposure to Padcev does not induce a downregulation of Nectin-4. Nectin-4 is still present, but there is a mechanism of resistance that is related to the payload. That's why we think that by shifting the mechanism of action to a topo-1 inhibitor, which is Exatecan, is a good approach so that we can first have a sequential approach. We can target patients who have been pre-exposed to PADCEV because we're having an orthogonal killing mechanism. Also, the topo-1, like Exatecan, has a good advantage over MMA. That is that it has a very good bystander effect. Using the linker that we have designed, which is very hydrophilic, that is masking the hydrophobicity of the Exatecan, at least in preclinical models, we have shown that we can have a very good bystander effect, which allows us to have efficacy in a tumor model where the expression of Nectin-4 is heterogeneous. That's something that we can observe in many more tumor types. Another differentiating factor on our product is coming from the binder, the antibody by itself. It is targeting a different epitope than Enfortumab and most of the ADC that are around. It is also allowing us to target low expressors. We are having a very good internalization rate. In all our preclinical models, we are showing that we can have efficacy where the other antibodies do not work at all. When there is a high level of expression of Nectin-4, I would say it is not really discriminating compared to all the antibodies, but in the low expressor, we are really having a very strong efficacy. That is why we think that it could potentially translate into the clinic into really a broader application for the antibody across multiple tumor types, where so far PADCEV has not shown really good results. Yeah, and I think if you apply that then from a clinical perspective, that allows you to develop the product in a couple of interesting ways. The first one is to go into a PADCEV resistance population where you can envisage a relatively small development program, potential accelerated approval from FDA, a really fast way to bring the product to market. If you go into one of the other tumor types that Yannis was talking about with the low or moderate levels of expression of Nectin-4, it gives you the opportunity to go into a significant tumor type where there is not the same level of competition, where you could go in and basically develop this product into a very significant product. It really gives you two avenues where you can develop the product from a clinical perspective in a really effective way. Could you provide an update on Leukotumab's regulatory pathway following recent FDA interactions? Yeah, I can do that. We have had a couple of interactions with FDA. Towards the end of last year, we had a discussion about an accelerated path to approval, and we agreed on a path at a high level. We basically agreed on the high-level elements of a confirmatory study that will be required to do that. Probably the most important thing in light of Project Optimus is that we agreed on a single dose to take into the phase III, which is really important. We also agreed that we could test in the phase III in an earlier line of therapy, so we could go in a second line plus line of therapy. Very importantly, we could go in an all-comers population. We had basically had different cohorts for KIR3DL2 overexpression, high expressors and low expressors in the phase II. For the phase III, as we saw activity in both of those groups, we can basically go straight with an all-comers study and obviously check for KIR3DL2 retrospectively. That allows us to basically move reasonably quickly with that. Subsequent to that discussion, we have had a Breakthrough Therapy Designation from FDA for the Sézary syndrome indication, which is facilitating our interactions with FDA today and making sure that things are moving forward in a very timely way. We are now in discussions with FDA to absolutely finalize the protocol for the confirmatory study. We hope to initiate that study towards the end of this year or early next year, which will allow us, once we have the study up and going and we have a recruitment trajectory into the study, to actually submit a BLA for the Sézary syndrome indication, which will then confirm and get the full approval for the whole of cutaneous T-cell lymphoma, which is Sézary and mycosis fungoides, once we have the results from that confirmatory study. It is moving fast and in a good way with FDA, and we're excited to take the next steps. At ASCO this year, you presented long-term follow-up data for IPH4102 and CTCL. What were the key takeaways from this data? The key takeaways from the ASCO presentation, which was on Monday this week, was basically that the data continues to get better with time. What we see is the objective response rate has gone up from the original primary endpoint cut of the study. The duration of therapy continues to increase, and we see some very exciting things there. We have patients now who have been on the drug for over five years, which I think is phenomenal if you think of the severity of this disease, particularly Sézary syndrome, that you can maintain patients on the drug for such a long period of time. I think it is a testament to the safety profile of the product and the tolerability. This product is basically making a very significant difference for patients. We are excited to be taking that forward. The results that we presented at ASCO were actually the basis for the breakthrough therapy designation with FDA. FDA has seen this data, and obviously, they comment on it with the BTD. I think that, again, is a reflection on the data and the quality of it and the impact that it can have for patients. We are looking forward to actually taking that forward in forms of a BLA once we have the confirmatory study up and running and being able to go to next steps. On your last earnings call, you mentioned exploring strategic options and partnerships for IPH4102. Could you elaborate on the types of options you are considering? Yannis, you want to take this one? Yeah, as we mentioned, I would say our preferred path forward would be to find a partner to help us to earn the phase III and to commercialize this drug. That's something that we are currently pursuing quite actively with several advanced discussions, I would say, with a mid-size type of pharma. There is really something, as we really believe in this drug, we think that the potential is even greater than what we can calculate today based on the previous history of CTCL treatment. It's not something that it's not a drug where we will accept a bad deal. We are really also exploring in parallel other ways to finance the phase III. Because at the end of the day, I mean, without disclosing too much details on the phase III, we are still working on it. It's something that is really within our capacity to execute. We are currently also looking at an alternative way to finance the phase III and execute it ourselves. What is the latest update on Leukotumab's development in PTCL? In PTCL, this is an indication that we've actually been exploring through a collaborative trial group. We're working with the LISARC group in France, and they have been investigating Leukotumab in combination with chemotherapy with the Gemox regimen. They've been randomizing Gemox versus Gemox plus Leukotumab. That study is progressing very nicely. We're expecting that the collaborative trial group will be presenting data probably sometime later this year or early next year. We're looking forward to that. We're very, very confident that we're going to see something positive for Leukotumab from that study. Just to remind you of PTCL or peripheral T-cell lymphoma, it's a significantly bigger indication. In cutaneous T-cell lymphoma, which is Sézary's and mycosis fungoides, we're about 5,000 patients that we're looking at in the large seven markets. With PTCL, we're looking at close to 20,000 patients across those same seven markets. It has about four times the potential eligible patients that could actually be eligible to be treated with IPH4102. It is an exciting lifecycle management opportunity, and it is something that is important to partners when we are having discussions about a potential partnership for the cutaneous T-cell lymphoma. We are very pleased that the study with LYSARC is moving quickly and in a good way. We look forward to seeing the data, hopefully sometime soon. What is the current status of Monalizumab's clinical development? Yeah, so Monalizumab is, I would say, our latest stage product. It's in a collaboration with AstraZeneca. Just to remind you of a few of the details of that collaboration, it is basically a partnership where we've already received substantial milestones, over $450 million already. We're eligible for another $825 million milestones associated with the deal in the case of the study being positive, the standard commercial regulatory development time milestones. The product is actually in a large phase III study. It's a 1,000-patient study in combination with Durvalumab from AstraZeneca. On clinicaltrials.gov, it's scheduled to read out in May 2026. We're a little under a year away from that potential phase III readout. Obviously, that would be a significant event for Innate Pharma with all of the positive ramifications of a positive study. It's something we're looking forward to with excitement and anticipation. We feel that the hypothesis behind the study was further validated at ASCO. The NeoCOAST-2 data was presented by AstraZeneca. If you look in the PD-L1 high category of that study, the regimen of Durvalumab plus Monalizumab was the best regimen out of the regimens that were being tested and was showing a significant advantage on top of Durvalumab. That gives us a certain element of confidence looking forward to the future and to that future readout next year. What should we take from the most recent data presented at ASCO? The most recent data at ASCO, it was basically what I was just alluding to. That is the NeoCOAST-2 data. It validates the hypothesis. I think based on the fact that in the PD-L1 high overexpressors, it was the best regimen, it basically gives us a lot of confidence in the PAC9 study and that we'll hopefully be seeing a positive readout in May next year. Moving on to more financials, what is your current cash way following Sanofi's $15 million equity investment? Do you anticipate any near-term financing needs? From a cash perspective, we've communicated with our Q1 results that we have a cash runway to mid-2026. That was excluding the $15 million of equity investment from Sanofi. We're likely to use that $15 million equity investment in a number of ways to potentially extend the cash runway to some degree, but also to potentially accelerate some of our programs that we have ongoing so that we can deliver results more quickly. Yeah, I think that will be all I would have to say on the cash runway. For the final question we have prepared, what are the key catalysts and milestones we should be watching for in 2025 and beyond? I think we've covered them all in the presentation, but just to summarize them, the key catalysts, I think Leukotumab partnership would be something that's important. Hopefully, there will be some associated upfronts with a partnership that we would put in place. Obviously, in longer term, some milestones, royalties, etc. We have data readouts from our ADC, the Nectin-4 targeted ADC, sometime towards the end of the year or early next year, safety and efficacy. Also, data readouts from IPH6501 in the B-cell lymphoma indication. Again, hopefully, safety and some hints of efficacy, again, before the end of the year or early next year. The final data readout was what I was talking about previously, which is Monalizumab. We have the primary event, the primary endpoint, which will read out in May next year. They're really the four key inflection points for Innate Pharma, which. Our fireside chat. Okay, thank you. Thank you.